Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Mais filtros

Base de dados
Ano de publicação
Tipo de documento
País de afiliação
Intervalo de ano de publicação
1.
Neuroscience ; 141(1): 433-42, 2006 Aug 11.
Artigo em Inglês | MEDLINE | ID: mdl-16690218

RESUMO

Temporomandibular disorder is a major health problem associated with chronic orofacial pain in the masticatory muscles and/or temporomandibular joint. Evidence suggests that changes in primary afferents innervating the muscles of mastication may contribute to temporomandibular disorder. However, there has been little systematic study of the mechanisms controlling the excitability of these muscle afferents, nor their response to inflammation. In the present study, we tested the hypotheses that inflammation increases the excitability of sensory neurons innervating the masseter muscle of the rat and that the ionic mechanisms underlying these changes are unique to these neurons. We examined inflammation-induced changes in the excitability of trigeminal ganglia muscle neurons following intramuscular injections of complete Freund's adjuvant. Three days after complete Freund's adjuvant injection acutely dissociated, retrogradely labeled trigeminal ganglia neurons were studied using whole cell patch clamp techniques. Complete Freund's adjuvant-induced inflammation was associated with an increase in neuronal excitability marked by a significant decrease in rheobase and increase in the slope of the stimulus response function assessed with depolarizing current injection. The increase in excitability was associated with significant decreases in the rate of action potential fall and the duration of the action potential afterhyperpolarization. These changes in excitability and action potential waveform were associated with significant shifts in the voltage-dependence of activation and steady-state availability of voltage-gated K(+) current as well as significant decreases in the density of voltage-gated K(+) current subject to steady-state inactivation. These data suggest that K(+) channel subtypes may provide novel targets for the treatment of pain arising from inflamed muscle. These results also support the hypothesis that the underlying mechanisms of pain arising from specific regions of the body are unique suggesting that it may be possible, if not necessary to treat pain originating from different parts of the body with specific therapeutic interventions.


Assuntos
Inflamação/fisiopatologia , Músculo Masseter/inervação , Músculo Masseter/fisiopatologia , Neurônios Aferentes/fisiologia , 4-Aminopiridina/farmacologia , Potenciais de Ação/fisiologia , Análise de Variância , Animais , Relação Dose-Resposta à Radiação , Estimulação Elétrica/métodos , Adjuvante de Freund/toxicidade , Inflamação/induzido quimicamente , Masculino , Condução Nervosa/efeitos dos fármacos , Condução Nervosa/fisiologia , Condução Nervosa/efeitos da radiação , Técnicas de Patch-Clamp/métodos , Bloqueadores dos Canais de Potássio/farmacologia , Ratos , Ratos Sprague-Dawley , Limiar Sensorial/efeitos dos fármacos , Limiar Sensorial/fisiologia , Limiar Sensorial/efeitos da radiação , Gânglio Trigeminal/citologia , Gânglio Trigeminal/fisiopatologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA